Evidence map›Paper›PMID 19139272›Full record

ArticleMolecular and cellular biology2009

Aberrant double-strand break repair resulting in half crossovers in mutants defective for Rad51 or the DNA polymerase delta complex.

Catherine E Smith, Alicia F Lam, Lorraine S Symington

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  3. POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Break-induced replication: unraveling each step.Trends in genetics : TIG · 2022
    Review
  13. Article
  14. Mechanistic origins of diverse genome rearrangements in cancer.Seminars in cell & developmental biology · 2022
    Review
  15. Article
  16. Break-induced replication mechanisms in yeast and mammals.Current opinion in genetics & development · 2021
    Review
  17. Article
  18. Repair of DNA Breaks by Break-Induced Replication.Annual review of biochemistry · 2021
    Review
  19. Investigation of Break-Induced Replication in Yeast.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  20. Article

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 2 countries.

Catherine E SmithColumbia University College of Physicians & Surgeons, Department of Microbiology, New York, NY 10032-2704, USA.
Alicia F Lam
Lorraine S Symington
Columbia College · CA

Funding

Mechanisms of Homologous Recombination in YeastR01GM041784 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SYMINGTON, LORRAINE S · 1989 to 2017
$7.8M
MECHANISMS OF DOUBLE STRAND BREAK REPAIR IN YEASTR01GM054099 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SYMINGTON, LORRAINE S · 1997 to 2009
$2.5M
NIGMS NIH HHS GM041784NIGMS NIH HHS GM054099NIGMS NIH HHS R01 GM041784NIGMS NIH HHS R01 GM054099
6 · The paper itself

Abstract

Homologous recombination is an error-free mechanism for the repair of DNA double-strand breaks (DSBs). Most DSB repair events occur by gene conversion limiting loss of heterozygosity (LOH) for markers downstream of the site of repair and restricting deleterious chromosome rearrangements. DSBs with only one end available for repair undergo strand invasion into a homologous duplex DNA, followed by replication to the chromosome end (break-induced replication [BIR]), leading to LOH for all markers downstream of the site of strand invasion. Using a transformation-based assay system, we show that most of the apparent BIR events that arise in diploid Saccharomyces cerevisiae rad51Delta mutants are due to half crossovers instead of BIR. These events lead to extensive LOH because one arm of chromosome III is deleted. This outcome is also observed in pol32Delta and pol3-ct mutants, defective for components of the DNA polymerase delta (Pol delta) complex. The half crossovers formed in Pol delta complex mutants show evidence of limited homology-dependent DNA synthesis and are partially Mus81 dependent, suggesting that strand invasion occurs and the stalled intermediate is subsequently cleaved. In contrast to rad51Delta mutants, the Pol delta complex mutants are proficient for repair of a 238-bp gap by gene conversion. Thus, the BIR defect observed for rad51 mutants is due to strand invasion failure, whereas the Pol delta complex mutants are proficient for strand invasion but unable to complete extensive tracts of recombination-initiated DNA synthesis.

Indexed as

DNA Breaks, Double-StrandedChromosome BreakageChromosomes, FungalDNA Polymerase IIIDNA RepairDNA ReplicationGene Expression Regulation, FungalMutationRad51 RecombinaseRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA Polymerase IIIRad51 RecombinaseSaccharomyces cerevisiae Proteins

Identifiers

PMID19139272
PMCPMC2648250
OpenAlexW2113908436

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.